Page 431 - Environmental Nanotechnology Applications and Impacts of Nanomaterials

Toxicological Impacts of Nanomaterials 411

anatase TiO treatments but not with >200 nm anatase or 200 nm
2
rutile treatments. These results indicated that nanoscale anatase
could induce oxidative damage to lipids and DNA. Finally, cell treatments
with anatase TiO 2 nanoparticles showed an increase in nitric oxide
levels and hydrogen peroxide that probably leads to chromosomal
damage. Iron and titanium oxide nanoparticles have also been shown
to distort mitochondria, leading to a mitochondrial activity disruption
that increases oxidative burst (Long et al., 2006). These results are
strongly correlated with the size of the particles, the smaller particles
being the more destructive. Thus, the anatase form of TiO could induce
2
reactive oxygen species and chromosome damage in vitro in the absence
of UV photoactivation. Futhermore, rutile and anatase forms differ in
their oxidative properties following UV irradiation (Gurr et al., 2005).
The pulmonary effects of TiO particles have been well documented
2
in vivo. Several investigators have shown that 20–30 nm TiO particles
2
cause pulmonary inflammation in laboratory animals (Ferin et al., 1990;
Ferin et al., 1992; Oberdoerster et al., 1994; Oberdoerster et al., 1995).
Rat cells did not respond to 1-µm TiO particles in suspension (Stringer
2
et al., 1996), which strongly suggested that an enhancement of biolog-
ical reactivity and/or cytotoxicity occurs as the particle size decreased
from the micrometer to the nanometer range (Cheng et al., 2004). When
the inflammatory responses following intratracheal instillation of ultra-
fine particles of Co, Ni, and TiO in male rats were compared, TiO par-
2
2
ticles were found to be the least toxic of these three materials (Zhang
et al., 1998).
Untreated TiO particles (hydrophilic surface) and silanized TiO par-
2
2
ticles (hydrophobic surface) were administered to rats and the inflam-
matory and genotoxic lung effects were recorded. Animals exposed to
untreated and silanized TiO particles showed no signs of inflammation
2
with TNF-α, fibronectin, and surfactant phospholipids (Rehn et al.,
2003). Immunohistochemical detection of 8-oxoguanine (8-oxoGua) by
a polyclonal antibody in the DNA of individual lung cells was conducted
on frozen sections of the left lobe of the lung. The amount of 8-oxoGua,
a marker of DNA damage, was at the same level as that of the controls
(Rehn et al., 2003). In contrast, nano-sized TiO without UV irradiation
2
has been shown to cause chronic pulmonary inflammation in rats in the
presence of alveolar macrophages (Oberdörster et al., 1992). Inhaled
ultrafine titanium dioxide particles induced the production of reactive
oxygen species in human in rat and human alveolar macrophages
(Rahman et al., 1997).
Other investigators have evaluated the acute lung toxicity in rats of
intratracheal instilled pigment grade TiO particles (rutile type approx-
2
imately 300 nm), nanoscale TiO rods (anatase 200 nm
35 nm) or
2
nanoscale TiO dots (anatase-10 nm) compared with a positive control
2